Cardiovascular disease is the major cause of death not only in western countries but also worldwide. The majority of adverse cardiovascular events develop due to the evolution of atherosclerotic lesions in coronary and cerebral arteries. The atherosclerotic process begins in childhood with the development of fatty streaks, which progress to fibrous plaques that may ultimately cause ischemic damage through thrombotic occlusions. Fatty streaks are focal regions of intimal thickening consisting of foam cells (lipid laden macrophages and monocytes), T lymphocytes, and vascular smooth muscle cells that have proliferated and migrated within the intima. Further accumulation of smooth muscle cells, macrophages, connective tissue, and lipid deposits transforms the fatty streak into a fibrous plaque. Advanced lesions are characterized by reactive fibrous caps, revascularization, and a necrotic core consisting of leukocytes, lipids and debris.
Abnormal growth of arterial smooth muscle cells is one of the most important contributing factors to the genesis of atherosclerosis. In response to pathological stimuli, smooth muscle cells initially migrate from the media layer to the intima layer of the arterial wall, and then proliferate within the intima layer. These events are instrumental to the induction of atherosclerotic deposition. Formation of atherosclerotic lesions in the intima layer occurs in a number of cardiovascular diseases including hypertension, atherosclerosis, myocardial ischemia, myocardial infarction and stroke (cerebrovascular accident). Therefore, prevention and/or retardation of the pathological stimulation of smooth muscle growth has become a critical objective of sustained cardiovascular health. Inflammatory responses, either acute or at chronic low levels, exacerbates and accelerates the elaboration and progression of atherosclerotic lesions.
Cardiovascular disease may be treated or alleviated in a number of ways. Preventative medicine contributes significantly toward reducing the global incidence of cardiovascular disease. These preventative measures often encompass health education, counseling, and monitoring of biological parameters. Many individuals, however, take various prescription oral medications, either as a result of cardiovascular disease or as a preventative measure.
Additionally, most orally administered, biologically active, substances must pass from the digestive system into the bloodstream in order to attain bioavailability and therapeutic efficacy. Upon entering the bloodstream, biologically active substances circulate to cells, organs, and tissues, exerting their biological effects. The concentrations of these substances in blood typically vary over time.
In general, serum levels peak shortly after oral administration, followed by achievement of steady state and a gradual decline in effective concentrations as the substance is metabolized. Biologically active substances maintain greatest efficacy when their blood levels are maintained at constant levels or within desired concentration ranges.
An unmet health need exists for a safe and effective method of alleviating cardiovascular abnormalities, and those associated with chronic or low level inflammatory responses.
In particular, individuals and healthcare professionals alike continue to seek an oral supplement, which promotes lowered levels of “bad” cholesterol or low-density lipoprotein (LDL).
The present invention and its embodiments meets and exceeds these objectives.